Insulin induces fatty acid desaturase expression in human monocytes

Scand J Clin Lab Invest. 2011 Jul;71(4):330-9. doi: 10.3109/00365513.2011.566350. Epub 2011 Mar 17.

Abstract

Increasing evidence suggests that fatty acid desaturases, rate-limiting enzymes in unsaturated fatty acid biosynthesis, are important factors in the pathogenesis of lipid-induced insulin resistance. The conversion of dihomogamma linolenic acid (DGLA) into arachidonic acid (AA) in human plasma phospholipids has been shown to be regulated by insulin, suggesting a role for insulin in fatty acid desaturase 1 regulation. However insulin's role in monocyte inflammation associated with obesity and lifestyle disease development is uncertain. We therefore investigated if insulin is able to induce expression of stearoyl-CoA desaturase (SCD, Δ9 desaturase), fatty acid desaturase 1 (FADS1, Δ5 desaturase), and fatty acid desaturase 2 (FADS2, Δ6 desaturase), as well as the sterol regulatory element binding transcription factor 1-c (SREBP-1c) in monocytes. Here, for the first time, we demonstrate that THP-1 monocytes are insulin-responsive in inducing expression of SCD, FADS1, and FADS2 in a time- and dose-dependent manner. Understanding secondary consequences of postprandial hyperinsulinemia may open up new strategies for prevention and/or treatment of obesity-related metabolic complications.

MeSH terms

  • Cell Line
  • Culture Media
  • Delta-5 Fatty Acid Desaturase
  • Fatty Acid Desaturases / genetics
  • Fatty Acid Desaturases / metabolism*
  • Humans
  • Insulin / pharmacology*
  • Monocytes / drug effects*
  • Monocytes / metabolism
  • Stearoyl-CoA Desaturase / genetics
  • Stearoyl-CoA Desaturase / metabolism
  • Sterol Regulatory Element Binding Protein 1 / genetics
  • Sterol Regulatory Element Binding Protein 1 / metabolism
  • Transcription, Genetic
  • Up-Regulation

Substances

  • Culture Media
  • Delta-5 Fatty Acid Desaturase
  • Insulin
  • Sterol Regulatory Element Binding Protein 1
  • Fatty Acid Desaturases
  • Stearoyl-CoA Desaturase
  • FADS1 protein, human
  • FADS2 protein, human